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Activation of c-Jun N-Terminal Kinase and p38 in an Alzheimer's Disease Model Is Associated with Amyloid Deposition
Open accessAbstract
The mechanisms by which neurons and synapses are lost in Alzheimer's disease (AD) are not completely understood. To characterize potential signaling events linked to AD pathogenesis, activation-specific antibodies were used to examine mitogen-activated protein kinase (MAPK) kinase pathways at various ages in mice transgenic for human amyloid precursor protein-695 with the Swedish familial AD mutations (Tg2576) and homozygous for a P264L familial AD mutation introduced by targeting of the presenilin-1 gene (PS1(P264L)). Although the c-Jun N-terminal kinase (JNK) and p38 pathways were significantly activated in the cortex at both 7 and 12 months of age, there was no significant activation of the extracellular signal-regulated kinase pathway. MAPK kinase-4, an upstream activator of JNK, was also significantly activated at 7 and 12 months, whereas c-Jun, a downstream effector of JNK-associated apoptotic signaling, was not induced. The lack of c-Jun activation is consistent with the absence of neuronal loss in both cortex and hippocampal CA1 at 12 months. The JNK activation was localized to amyloid deposits, within neurites containing phosphorylated tau. Synaptophysin was quantified biochemically as a measure of synaptic integrity and was significantly reduced in an age-dependent manner in the Tg2576/PS1(P264L) cortex but not in either PS1(P264L) or Tg2576 cortex. Stress-responsive MAP kinase pathways were activated in the brain of the Tg2576/PS1(P264L) AD model, and this activation was coincident with the age-dependent increase in amyloid deposition, tau phosphorylation, and loss of synaptophysin.
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“Since p38MAPK is a major regulator of SASP [209], it is not surprising that a number of key components of SASP appear to be up-regulated in AD [210,211].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [211]
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CD14 and Toll-Like Receptors 2 and 4 Are Required for Fibrillar Aβ-Stimulated Microglial Activation
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Metadata
- Authors
- Savage, M. J., Lin, Y.-G., Ciallella, J. R., Flood, D. G., & Scott, R. W.
- ORCID
- Scott, Richard W.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2002-05-01
- Volume
- 22
- Issue
- 9
- Pages
- 3376-3385
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6758401
- OpenAlex
- W1558509021
- Cited by
- 291
- References
- 61
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 6 · 2023: 11 · 2022: 10 · 2021: 8 · 2020: 8 · 2019: 15 · 2018: 8 · 2017: 8 · 2016: 16 · 2015: 9 · 2014: 14 · 2013: 9 · 2012: 6
- FWCI
- 12.81
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, c-Jun N-terminal kinase, p38 MAPK, amyloid deposition, MAPK signaling, Tg2576 mice, amyloid precursor protein, MAPKAPK4, c-Jun, tau phosphorylation, synaptophysin, synaptic integrity, neuronal loss, hippocampal CA1
- MeSH terms
- Aging, Alzheimer Disease, Amyloid, Animals, Cell Count, Cerebral Cortex, Disease Models, Animal, Enzyme Activation, Hippocampus, Humans, Immunohistochemistry, Membrane Proteins, Mice, Transgenic, Neurons, Phosphorylation, Signal Transduction, Neurites, Amyloid beta-Protein Precursor, Synaptophysin, tau Proteins, Gene Targeting, Amino Acid Substitution, Mitogen-Activated Protein Kinases, JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases, Mice, Presenilin-1
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